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SAGE KE Paper


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#1 kevin

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Posted 13 February 2004 - 08:24 AM


A study confirming the findings of Susan Kenyon's lab that heat shock proteins also play a significant role in extending lifespan have been confirmed independently in this article entitled "Search for Methuselah Genes Heats Up" at the SAGE Knowledge Environment.

Article.

You need a subscription to read the entire thing but if someone would like a look at my copy, let me know.

Juicy bits..

Over the past 10 years, molecular geneticists have identified signal transduction pathways that regulate longevity in yeast, worms, flies, and mice. The inactivation of these pathways causes changes in gene expression that are normally associated with entry into periods of starvation. Among the genes that are consistently up-regulated in long-lived mutants are those that encode stress resistance proteins, specifically proteins that protect against oxidative and thermal damage. Until recently, expression of pro-longevity stress resistance genes in the worm Caenorhabditis elegans was believed to be mostly under the control of the DAF-16 transcription factor (see Johnson Review). In a recent article in Molecular Biology of the Cell, Morley and Morimoto (1) show that stress resistance genes that extend longevity are also regulated by the transcriptional activator heat shock factor 1 (HSF-1) independently of DAF-16, confirming recent studies by the Kenyon laboratory (2) (see "Vital Collaboration").


The links between the pathways induced by CR and the role which protein degradation, sugar metabolism and free radical generation are being elucidated with changes in single tissues of the levels of these proteins having body wide effects. I especially like this closing paragraph statement which points out the power of the converging efforts in biotech to understand the causes of aging..



The combination of studies aimed at separating the cell-autonomous from cell-nonautonomous effects of longevity-enhancing proteins in multicellular organisms, with further studies in unicellular S. cerevisiae, other animal systems, and mammalian cell cultures, should soon illuminate the molecular and cellular networks responsible for the regulation of life span in eukaryotes.


We'll find out what the 'tricky' DNA is up to yet..

#2 reason

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Posted 13 February 2004 - 09:38 AM

<poke> Want to put together an analysis for Fight Aging ?</poke>

Reason
Founder, Longevity Meme
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http://www.longevitymeme.org

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#3 Cyto

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Posted 14 February 2004 - 10:32 PM

Well I'm sorry for killing the conversation.

The Hsp70 connection with Bax is "spit new." hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondria So I wanted to chime in about it along with other elucidations.

Edited by CarboniX, 17 February 2004 - 06:07 AM.


#4 kevin

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Posted 15 February 2004 - 08:24 PM

heh.. :)

for my own part.. you didn't kill the conversation.. but did serve to illustrate again just how much I need to learn to catch up with you.. :)

A review of the apoptotic process and the players involved was necessary for me to understand your post..

It seems that there are lot of instances where cells commit suicide through apoptosis which if it could be avoided would be very beneficial for the organism as a whole. There are good reasons for wanting a cell to self-destruct, ie. cancer or just natural growth, but in some cases it seems an unnecessary response to trauma or disease, and most likely aging as well, where imbalances between cell death and cell replacement lead to weakening of tissues and funtion.

I found an interesting article on Eurekalert which describes yet another protein called 'humanin' which also seems to interfere with Bax's ability to form pores in the mitochondrial membrane.

http://www.eurekaler...i-tpp050903.php

Manipulating apoptosis (cell death) is certainly going to figure VERY prominently in keeping tissues functioning optimally and there are bound to be therapeutics on the not too distant horizon.

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#5 Cyto

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Posted 17 February 2004 - 05:58 AM

Thanks again for the Humanin info.

Speaking of Bax-related issues, today happened to have some Bax in it [lol].

Team of LIAI Scientists Discover New Way Protein Kills Cancer Cells

In a paper (Direct Activation of Bax By p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis, Science, February 2004) published today in the scientific journal Science, Douglas Green, Ph.D., and a team of LIAI researchers have discovered that the protein, p53, can not only suppress a tumor cell when present in the nucleus of the cell, but can also cause apoptosis, or cell death, when present in the cytoplasm


Muuahhahha!




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